Monday, November 04, 2024

Rapeseed oil for weight loss (3) Canola oil vs butter round two

Now to get down to the nitty gritty of the first anomaly in the paper


The oddity is the blip downwards of weight in canola fed rats, highlighted by the red oval on the graph:
















which needs to be read in conjunction with the food intakes in this graph, also highlighted by a red oval:














I've copied the food intake graph and laid it over the weight graph to make it a bit clearer:




















Because the red graph is in grams of food I've annotated the important energy intakes next to the related data points. Obviously the switch from chow to high fat diet (fine orange line) massively alters the caloric intake despite the weight eaten being the same on the day before and after the switch.

Interminable aside: if any paper gives you the caloric density of any food used you are assured that the group are idiots, even if they are very, very clever idiots. They believe you can fool a rat's hypothalamus in to over-consuming calories by increasing the caloric density of the food. Or fool it in to under-consuming calories by diluting them down with sawdust or the equivalent (usually cellulose). As if evolution is that gullible. Do not, under any circumstances, accept any of such a group's ideas about satiety, food intake or bodyweight. Ever. End aside.

Anyhoo. On day one the high fat fed rats increased their energy intake from around 227kJ (55kcal) to 355kJ (85kcal), a rise of ~56%. I find this impressive and in the same league as the Schwartz lab rats on D12492, who increased their caloric intake by ~87% on day one in this venerable graph:






















In Protons terms the canola oil fed rats still used 227kJ for running their metabolism but "lost" 128kJ in to their adipocytes via the enhanced insulin signalling of linoleic acid (LA) and alpha linolenic acid (ALA) due to their low F:N ratios. The rats needed 227kJ, they lost 128kJ so needed to replace those 128kJ, therefore they ate 227+128 = 355kJ. They stopped at 355kJ because that's when they stopped being hungry. Overall weight did not change because 227kJ of chow weighs the same as 355kJ of the canola oil diet (Hmmm, chance or pilot study????). 128kJ is about 3g of fat gain.

Simple.

What happened next is much more exciting. On day two of the canola oil diet the rats weren't hungry. They only ate 155kJ that day. The weight of food eaten dropped by ~13g, and so did the weight (~10g) of the rats, food is heavy, they ate less, they weighed less. But they still needed those 227kJ to run their metabolism. They ate until they weren't hungry, that's what they do. Why weren't they hungry?

They must have accessed the full 227kJ that they needed, otherwise they would still have been hungry. They obtained the missing 72kJ from their adipocytes. Without "trying", without being hungry. Remember, they always eat to satiety.

The logical explanation is that there was an acute drop in insulin signalling in their adipocytes which released 72kJ worth of FFAs, which meant that there was no need to eat the 72kJ's worth of food needed to reach the full 227kJ to run metabolism. 72kJ is the energy available from about 2g of fat.

From the Protons perspective acute loss of insulin signalling is a standard effect of reduced mitochondrial membrane potential caused by uncoupling. PUFA uncouple. At high intakes this over rides the obesogenic effect of their reduced F:N ratio.

The blip of weight down then back up again mostly reflects food weights with a lesser contribution from adipose weights, but the latter adipose changes are the factor responsible for the hunger changes which drive the food intake changes.

Uncoupling explains the blip. The only thing which surprised me was how rapidly the effect kicked in. I would have expected that about a week would be about the time scale but here it was 48h. Those are the data. I have to revise my views in the light of it. You don't often get given a gift-horse (of daily food intakes and daily body weight changes) to consider examining the mouth of!

The following day the rats increased their food intake. Under steady growth the rats still needed the standard 227kJ/d plus some extra for uncoupling losses. Adipocyte size does not continue to shrink because the uncoupling using biological uncoupling proteins is ATP dependent, low intra mitochondrial ATP reduces the effectiveness of uncoupling proteins. This is distinctly different from chemical uncoupling to which there is no upper limit and so these can give extreme weight loss or even death.

The rats still needed 227kJ/d for metabolism and 62kJ/d for uncoupling, hence 289kJ/d. This happened pretty consistently throughout the rest of the high fat period. They stayed slim but not too slim.  Despite eating around 20% extra in calories compared to the chow fed mice.

Peter

There is another very strange/interesting feature on the food intake graph. I'll see when I can find time to describe it.

3 comments:

mct4health said...

Interesting as always. It looks like AMPK activation (ACC phosphorylation) after switch to canola, definitely not activated by butter. Could 13% of ALA be that effective? I think it can, acetate and ACSS2 as in many cases before :-)
Btw, additional released fat cannot be burned without ACC phosphorylation.
Jaromir

karl said...

First, we might want to point out that the name "Canola" was a rebranding of rapeseed oil so people would think it was safe.

The uncoupling is part of what I've been thinking about lately - is the cause of much of obesity the lack of uncoupling - some environmental effect that make us run cooler than we should when there is an abundance of energy available?

I've talked to countless people that complain of cold intolerance when they are trying to diet. T3 drops with fasting.

https://www.sciencedirect.com/science/article/pii/S001457930300320X

As usual, there is a pretty good list of confounding control loops that effect coupling - as well as fusion and fission of MT.

mct4health said...

Peter, couldn't find if the diet contained sugar. If yes, then it would explain LPS poisoning with butter diet, and also lactate as MCT1 transporter activator for acetate effect acceleration.
Jaromir